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- W3167185283 abstract "The inflammasome is a newly discovered molecular platform required for the caspase-1 activation and maturation of IL-1β. IL-1β is the most active cytokine in acute lung injury patients. Recently it has been reported that reactive oxygen species (ROS) are required for purinergic P2X7 receptor (P2X7R)-mediated NALP3 inflammasome activation. Our previous results suggest that suppressor of cytokine signaling-1 (SOCS-1) functions as negative regulator in ROS-induced apoptotic responses by inducing ASK-1 degradation. Thus, we hypothesized that the toxic effects of hyperoxia could be mediated by ASK-1-induced P2X7 mediated inflammasome and that the protective effects of SOCS-1 could be due, at least in part, to its ability to suppress inflammasome response. To test this hypothesis we administered SOCS–1 adenovirus (Ad-SOCS-1) into the lung and exposed mice to 100%O2. Ad-GFP infected mice were used as controls. Inflammasome complex formation was assessed by immunoprecipitation and western blot. Ad-SOCS-1 mice lived significantly longer in hyperoxia when compared to Ad-GFP. After 72 hours of hyperoxia, inflammasome was activated and associated with enhanced caspase-1and IL-1 β cleavage in the Ad-GFP mice but inflammasome assembly was abolished in the Ad-SOCS-1 mice with significant decrease in caspase-1and IL-1 β cleavage. These findings suggest that SOCS-1 over-expressing mice are protected from hyperoxia-induced inflammation, which is associated with inactivation of inflammasome, thus demonstrating a critical role for SOCS-1 in inflammasome-mediated inflammation. (This work was funded by T32-HL007874)." @default.
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- W3167185283 date "2010-04-01" @default.
- W3167185283 modified "2023-09-27" @default.
- W3167185283 title "Suppressor of Cytokine Signaling‐1 Inhibits Hyperoxic Induced Inflammasome Activation" @default.
- W3167185283 doi "https://doi.org/10.1096/fasebj.24.1_supplement.796.1" @default.
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